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An experimental model for congestive heart failure after encephalomyocarditis virus myocarditis in mice
Abstract:
Severe myocarditis was induced in inbred BALB/c mice inoculated with the M variant of encephalomyocarditis (EMC) virus. The mortality rate was maximal on the fourth day, then decreased gradually, but increased again between the eleventh and fourteenth days. Gross myocardial lesions were seen on the surface of the ventricles in 62 of 125 mice (49.6%) after the fifth day. These myocardial lesions were observed more frequently in the dead mice (46 of 49, 93.9%). Cavity dimensions and wall thickness were measured in two groups of mice with myocarditis. On days 5-7, the cavity dimensions of the right (RV) and left (LV) ventricles in inoculated mice (0.92 +/- 0.51 mm and 1.21 +/- 0.18 mm, respectively) were significantly larger than those in controls (RV 0.54 +/- 0.17, LV 1.01 +/- 0.15; p less than 0.05). The wall thickness of the RV (0.46 +/- 0.09, controls 0.64 +/- 0.11; p less than 0.001) and the LV (0.97 +/- 0.13, controls 1.12 +/- 0.19; p less than 0.05) was significantly decreased. On days 8-14, dilatation of the LV was more pronounced (1.48 +/- 0.37, p less than 0.005) than during days 5-7, and the interventricular septum was also thinner. Pleural effusion, ascites and congestion of the lungs and liver were noted, and death seemed due to congestive heart failure. This study is the first documentation of congestive heart failure after viral infection is an experimental animal.
Insights
Encephalomyocarditis (EMC) virus infection in mice caused severe myocarditis, leading to congestive heart failure. This study is the first to document this outcome in an experimental animal model.
Area of Science:
- Virology
- Cardiology
- Pathology
Background:
- Viral infections can cause myocarditis, inflammation of the heart muscle.
- Encephalomyocarditis (EMC) virus is a known cardiotropic virus.
- Congestive heart failure is a serious complication of severe heart damage.
Purpose of the Study:
- To investigate the pathological effects of EMC virus infection on the heart in a mouse model.
- To document the development of congestive heart failure following viral myocarditis.
Main Methods:
- Inbred BALB/c mice were inoculated with the M variant of EMC virus to induce myocarditis.
- Mortality rates were recorded daily.
- Gross myocardial lesions were assessed post-mortem.
- Echocardiographic measurements of cardiac cavity dimensions and wall thickness were performed on days 5-7 and 8-14 post-infection.
Main Results:
- A high mortality rate was observed, peaking on day 4 and again on days 11-14.
- Myocardial lesions were present in 49.6% of mice, predominantly in those that died (93.9%).
- Inoculated mice showed significantly enlarged ventricular cavities and decreased ventricular wall thickness compared to controls.
- Progressive left ventricular dilatation and thinning of the interventricular septum were noted in later stages.
- Signs of congestive heart failure, including pleural effusion, ascites, and organ congestion, were observed.
Conclusions:
- EMC virus infection induces severe myocarditis and pathological cardiac remodeling in mice.
- Congestive heart failure is a direct consequence of viral myocarditis in this experimental model.
- This study provides the first evidence of viral-induced congestive heart failure in an experimental animal.
